Evidence map›Paper›PMID 11161378›Full record

ArticleBritish journal of cancer2001

Chromosomal changes during development and progression of prostate adenocarcinomas.

H Zitzelsberger, D Engert, A Walch, U Kulka, M Aubele, H Höfler, M Bauchinger, M Werner

Open access · hybridAbstract readComparative Study
In one paragraph

Article in British journal of cancer, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Molecular mechanisms involving prostate cancer racial disparity.American journal of clinical and experimental urology · 2017
    Review
  3. Molecular basis for prostate cancer racial disparities.Frontiers in bioscience (Landmark edition) · 2017
    Review
  4. Article
  5. Article
  6. The genomic landscape of prostate cancer.Frontiers in endocrinology · 2012
    Article
  7. CYP24A1 is an independent prognostic marker of survival in patients with lung adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011
    Article
  8. The candidate oncogene CYP24A1: A potential biomarker for colorectal tumorigenesis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010
    Article
  9. Molecular mechanisms involving prostate cancer racial disparity.American journal of translational research · 2009
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Identification of a gene frequently mutated in prostate tumors.Medical oncology (Northwood, London, England) · 2001
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

H ZitzelsbergerInstitute of Radiobiology, GSF-Forschungszentrum für Umwelt und Gesundheit GmbH, Ingolstäder Landstr. 1, Neuherberg, D-85764, Germany.
D Engert
A Walch
U Kulka
M Aubele
H Höfler
M Bauchinger
M Werner
Technical University of Munich · DEInstitute of Groundwater Ecology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal copy number changes were investigated in 16 prostate carcinomas, 12 prostatic intraepithelial neoplasias (PIN; 4 low-grade and 8 high-grade) adjacent to the invasive tumour areas, and 5 regional lymph node metastases. For this purpose, comparative genomic hybridization (CGH) was performed and a copy number karyotype for each histomorphological entity was created. CGH on microdissected cells from non-neoplastic glands was carried out on 3 different cases to demonstrate the reliability of the overall procedure. None of the non-neoplastic tissue samples revealed chromosome copy number changes. In PIN areas, chromosomal imbalances were detected on chromosomes 7, 8q, Xq (gains), and on 4q, 5q, 8p, 13q and 18q (losses). In the primary tumours, recurrent (at least 25% of cases) gains on chromosomes 12q and 15q, and losses on 2q, 4q, 5q, Xq, 13q and 18q became apparent. Losses on 8p and 6q as well as gains on 8q and of chromosome 7 were also detected at lower frequencies than previously reported. The pooled CGH data from the primary carcinomas revealed a novel region of chromosomal loss on 4q which is also frequently affected in other tumour entities like oesophageal adenocarcinomas and is supposed to harbour a new tumour suppressor gene. Gains on chromosome 9q and of chromosome 16 and loss on chromosome 13q were observed as common aberrations in metastases and primary tumours. These CGH results indicate an accumulation of chromosomal imbalances during the PIN-carcinoma-metastasis sequence and an early origin of tumour-specific aberrations in PIN areas.

Indexed as

Chromosome AberrationsAdenocarcinomaDisease ProgressionDNA, NeoplasmHumansIn Situ Hybridization, FluorescenceMaleNucleic Acid HybridizationPolymerase Chain ReactionProstatic NeoplasmsDNA, Neoplasm

Identifiers

PMID11161378
PMCPMC2363712
OpenAlexW2053079199

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.